ABSTRACT
This population-based, retrospective, cohort study describes a large methicillin-resistant Staphylococcus aureus (MRSA) epidemic caused by one strain (E1) in the greater Helsinki region. The epidemic comprised 210 cases at several hospitals, but was finally controlled. The study period ranged from June 1991 to December 2000. The epidemic peaked in 1993-1995 with 143 cases (68% of total cases). From August 1993, all MRSA-positive cases at the eight municipal hospitals were isolated and barrier nursed. Contacts were cohorted and screened for MRSA colonization. Decolonization treatment was administered to some chronic carriers. MRSA cases and contacts were identified in the joint patient register of the municipal hospitals from August 1993. The annual incidence of MRSA E1 in Helsinki City area per 100,000 inhabitants rose from 0.2 in 1991 to 13.6 in 1994. It decreased from 1995, reaching 0.7 per 100,000 in 2000. A jointly agreed policy on MRSA and timely co-operation between all units were essential for control of this epidemic.
Subject(s)
Cross Infection/prevention & control , Disease Outbreaks , Infection Control/methods , Methicillin Resistance , Staphylococcal Infections/prevention & control , Adult , Aged , Aged, 80 and over , Cohort Studies , Cross Infection/epidemiology , Cross Infection/etiology , Female , Finland/epidemiology , Humans , Incidence , Male , Medical Records , Medical Staff , Middle Aged , Registries , Retrospective Studies , Staphylococcal Infections/epidemiology , Staphylococcal Infections/etiology , Staphylococcus aureus/isolation & purificationABSTRACT
To study the interrelations between the changes of acute phase proteins and those of serum lipoproteins in acute infections we measured the concentrations of different lipoproteins, serum amyloid-A protein and C-reactive protein and activities of lipoprotein lipase and hepatic lipase during acute and convalescence phase and after complete recovery in 64 patients with infectious diseases (30 with viral infection and 34 with bacterial infection). The maximal decrements of both low density lipoprotein and high density lipoprotein cholesterol correlated significantly with the acute phase levels of C-reactive protein and serum amyloid-A protein. The acute phase concentration of very low density lipoprotein triglyceride correlated inversely to C-reactive protein level (r = -0.31, P less than 0.05) but not to serum amyloid-A protein level. Regression analysis showed that the concentration of C-reactive protein was a significant predictor of very low density lipoprotein triglyceride level in the acute phase of infection but not during convalescence. These results and the previous findings that C-reactive protein binds to low and very low density lipoproteins and that serum amyloid-A protein is associated with high density lipoprotein give credence to the view that C-reactive protein and serum amyloid-A protein interfere with the metabolism of serum lipoproteins during acute phase of infection.
